Helicobacter pylori infection and other bacteria in pancreatic cancer and autoimmune pancreatitis

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F61988987%3A17110%2F21%3AA2202DJP" target="_blank" >RIV/61988987:17110/21:A2202DJP - isvavai.cz</a>

Nalezeny alternativní kódy

RIV/00843989:_____/21:E0109187 RIV/65269705:_____/21:00074672 RIV/00216224:14110/21:00120117 RIV/00209805:_____/21:00078870

Výsledek na webu

<a href="https://www.webofscience.com/wos/woscc/full-record/WOS:000691097800005" target="_blank" >https://www.webofscience.com/wos/woscc/full-record/WOS:000691097800005</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.4251/wjgo.v13.i8.835" target="_blank" >10.4251/wjgo.v13.i8.835</a>

Jazyk výsledku

angličtina

Název v původním jazyce

Helicobacter pylori infection and other bacteria in pancreatic cancer and autoimmune pancreatitis

Popis výsledku v původním jazyce

Helicobacter pylori (H. pylori) is an infectious agent influencing as much as 50% of the world's population. It is the causative agent for several diseases, most especially gastric and duodenal peptic ulcer, gastric adenocarcinoma and mucosa-associated lymphoid tissue lymphoma of the stomach. A number of other, extragastric manifestations also are associated with H. pylori infection. These include neurological disorders, such as Alzheimer's disease, demyelinating multiple sclerosis and Parkinson's disease. There is also evidence for a relationship between H. pylori infection and such dermatological diseases as psoriasis and rosacea as well as a connection with infection and open-angle glaucoma. Generally little is known about the relationship between H. pylori infection and diseases of the pancreas. Most evidence about H. pylori and its potential role in the development of pancreatic diseases concerns pancreatic adenocarcinoma and autoimmune forms of chronic pancreatitis. There is data (albeit not fully consistent) indicating modestly increased pancreatic cancer risk in H. pylori-positive patients. The pathogenetic mechanism of this increase is not yet fully elucidated, but several theories have been proposed. Reduction of antral D-cells in H. pylori-positive patients causes a suppression of somatostatin secretion that, in turn, stimulates increased secretin secretion. That stimulates pancreatic growth and thus increases the risk of carcinogenesis. Alternatively, H. pylori, as a part of microbiome dysbiosis and the so-called oncobiome, is proven to be associated with pancreatic adenocarcinoma development via the promotion of cellular proliferation. The role of H. pylori in the inflammation characteristic of autoimmune pancreatitis seems to be explained by a mechanism of molecular mimicry among several proteins (mostly enzymes) of H. pylori and pancreatic tissue.

Název v anglickém jazyce

Helicobacter pylori infection and other bacteria in pancreatic cancer and autoimmune pancreatitis

Popis výsledku anglicky

Helicobacter pylori (H. pylori) is an infectious agent influencing as much as 50% of the world's population. It is the causative agent for several diseases, most especially gastric and duodenal peptic ulcer, gastric adenocarcinoma and mucosa-associated lymphoid tissue lymphoma of the stomach. A number of other, extragastric manifestations also are associated with H. pylori infection. These include neurological disorders, such as Alzheimer's disease, demyelinating multiple sclerosis and Parkinson's disease. There is also evidence for a relationship between H. pylori infection and such dermatological diseases as psoriasis and rosacea as well as a connection with infection and open-angle glaucoma. Generally little is known about the relationship between H. pylori infection and diseases of the pancreas. Most evidence about H. pylori and its potential role in the development of pancreatic diseases concerns pancreatic adenocarcinoma and autoimmune forms of chronic pancreatitis. There is data (albeit not fully consistent) indicating modestly increased pancreatic cancer risk in H. pylori-positive patients. The pathogenetic mechanism of this increase is not yet fully elucidated, but several theories have been proposed. Reduction of antral D-cells in H. pylori-positive patients causes a suppression of somatostatin secretion that, in turn, stimulates increased secretin secretion. That stimulates pancreatic growth and thus increases the risk of carcinogenesis. Alternatively, H. pylori, as a part of microbiome dysbiosis and the so-called oncobiome, is proven to be associated with pancreatic adenocarcinoma development via the promotion of cellular proliferation. The role of H. pylori in the inflammation characteristic of autoimmune pancreatitis seems to be explained by a mechanism of molecular mimicry among several proteins (mostly enzymes) of H. pylori and pancreatic tissue.

Druh

J_imp - Článek v periodiku v databázi Web of Science

CEP obor

—

OECD FORD obor

30204 - Oncology

Projekt

<a href="/cs/project/NU20-03-00126" target="_blank" >NU20-03-00126: Hostitelský mikrobiom ve vztahu k rozvoji Barrettova jícnu a adenokarcinomu jícnu</a><br>

Návaznosti

V - Vyzkumna aktivita podporovana z jinych verejnych zdroju

Rok uplatnění

2021

Kód důvěrnosti údajů

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Název periodika

World Journal of Gastrointestinal Oncology

ISSN

1948-5204

e-ISSN

—

Svazek periodika

13

Číslo periodika v rámci svazku

8

Stát vydavatele periodika

US - Spojené státy americké

Počet stran výsledku

10

Strana od-do

835-844

Kód UT WoS článku

000691097800005

EID výsledku v databázi Scopus

—